1. Two types of neurotransmitter receptors: ionotropic and metabotropic.
\na. Describe at least TWO structural differences between ionotropic and metabotropic
\nreceptors. Make sure you describe how each receptor exemplifies this difference.
\nb. For the two structural differences above, describe how each of these account for a
\nfunctional difference in the receptors.
\nc. Crystal structures of the muscarinic and nicotinic acetylcholine receptors are shown
\nbelow. Using your knowledge of their basic molecular structure, correctly label each
\nreceptor.
\n2. Norepinephrine is a unique neurotransmitter to study, as it has 4 receptors (\u03b11, \u03b12, \u03b21, and \u03b22)
\ncapable of coupling to the 3 main types of G proteins (Gs, Gi, and Gq).
\na. Illustrate the pathways for Gs and Gi after binding of norepinephrine.
\ni. Ascribe the correct receptor(s) to each pathway (one or more receptors may not
\nbe used, since it is Gq coupled).
\nii. Include the effectors and second messengers
\niii. For each pathway, indicate the net\/overall impact on ion channels and ion levels
\nin the neuron.
\n3. Neurotransmitter release is proposed to follow the Quantum Hypothesis.
\na. Define what is meant by \u201cquantum hypothesis.\u201d
\nb. How many vesicles are in a single quantum?
\nc. In your own words, what is quantal size? What is one way that quantal size can be
\nchanged?
\nd. In your own words, what is quantal content? What is one way that quantal content can
\nbe changed?
\ne. In an individual with hypocalcemia (low Ca2+), what effect would this have on quantal
\nsize at the NMJ? What about quantal content?
\n4. You are comparing the neuromuscular junction from a patient with LEMS, a condition in which
\nthey have auto-antibodies against presynaptic vg-Ca2+ channels (which will block these
\nchannels) to a patient with a condition MG in which they have auto-antibodies against nAChR
\n(which will block this receptor). Answer LEMS, MG, Neither, or Both to the following statements.
\na. If you depolarized the presynaptic terminal to stimulate ACh release, which would you
\nexpect to have a normal EPP?
\nb. If you added physiologic levels of ACh to the NMJ, which would you expect to have a
\nnormal EPP?
\nc. If you added botulinum toxin to the NMJ, which would you expect to have a normal
\nEPP?
\n5. Ca2+ was a recurring element across this part of the course: from glia, to its function as a second
\nmessenger, and its role in neurotransmitter exocytosis. Answer the questions below regarding
\nCa2+ handling in the cell and its important contributions to these processes.
\na. Name 2 ways that Ca2+ can enter the neuron cytoplasm from outside the cell or from
\nintracellular stores.
\nb. Why is it necessary to control Ca2+ concentrations at \u201crest\u201d?
\nc. Name 2 methods the cell uses to keep cytoplasmic Ca2+ concentrations low.
\nd. Describe 1 way in which Ca2+ acts as a second messenger.
\ne. Describe one method in which scientists can monitor Ca2+ concentrations in a cell
\nexperimentally.
\nf. Describe at least one method scientists could use to control Ca2+ concentrations in a
\ncell experimentally.<\/p>\n","protected":false},"excerpt":{"rendered":"
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